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Acyl-CoA synthetase long-chain family member 4

The protein encoded by this gene is an isozyme of the long-chain fatty-acid-coenzyme A ligase family. Although differing in substrate specificity, subcellular localization, and tissue distribution, all isozymes of this family convert free long-chain fatty acids into fatty acyl-CoA esters, and thereby play a key role in lipid biosynthesis and fatty acid degradation. This isozyme preferentially utilizes arachidonate as substrate. The absence of this enzyme may contribute to the mental retardation or Alport syndrome. Alternative splicing of this gene generates 2 transcript variants. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ACID, CAN, ACSL3, HAD, V1a
Papers on ACS4
Abscisic Acid Antagonizes Ethylene Production through the ABI4-Mediated Transcriptional Repression of ACS4 and ACS8 in Arabidopsis.
Huang et al., Beijing, China. In Mol Plant, Feb 2016
Further analyses showed that expression of the ethylene biosynthesis genes ACS4, ACS8, and ACO2 was significantly decreased in abi4-152 but increased in the knockout mutants, with partial dependence on ABA.
Acyl-CoA synthetase-4, a new regulator of mTOR and a potential therapeutic target for enhanced estrogen receptor function in receptor-positive and -negative breast cancer.
Podesta et al., Buenos Aires, Argentina. In Oncotarget, Jan 2016
Although the role of acyl-CoA synthetase 4 (ACSL4) in mediating an aggressive phenotype is well accepted, there is little evidence as to the early steps through which ACSL4 increases tumor growth and progression.
ACSL4 promotes prostate cancer growth, invasion and hormonal resistance.
Lee et al., New York City, United States. In Oncotarget, Dec 2015
Here, we examine the expression and function of the fatty acid activating enzyme, long-chain fatty acyl-CoA synthetase 4 (ACSL4), in PCa.
Inhibition of long-chain acyl-CoA synthetase 4 facilitates production of 5, 11-dihydroxyeicosatetraenoic acid via the cyclooxygenase-2 pathway.
Hara et al., Tokyo, Japan. In Biochem Biophys Res Commun, Oct 2015
Among ACSL enzymes, ACSL4 prefers arachidonic acid (AA) as a substrate and plays an important role in re-esterification of free AA.
A novel 47.2 Mb duplication on chromosomal bands Xq21.1-25 associated with mental retardation.
Huang et al., Shanghai, China. In Gene, Sep 2015
Ten genes (i.e., ZNF711, SRPX2, RAB40AL, MID2, ACSL4, PAK3, UBE2A, UPF3B, CUL4B, and GRIA3) in the duplication interval have been associated with mental retardation.
Human Haploid Cell Genetics Reveals Roles for Lipid Metabolism Genes in Nonapoptotic Cell Death.
Stockwell et al., Stanford, United States. In Acs Chem Biol, Aug 2015
Using massive insertional mutagenesis of haploid KBM7 cells we identified nine genes involved in small-molecule-induced nonapoptotic cell death, including mediators of fatty acid metabolism (ACSL4) and lipid remodeling (LPCAT3) in ferroptosis.
Long term vitamin A restriction improves meat quality parameters and modifies gene expression in Iberian pigs.
Óvilo et al., In J Anim Sci, Jun 2015
Regarding changes in gene expression, ACSL4, CEBPB, and IGF1 genes were upregulated (P < 0.0001, P < 0.0001, and P < 0.05, respectively) in the ER group in hepatic tissue, whereas CRABPII and SCD genes were upregulated (P < 0.05) in the same group in adipose tissue.
Global Transcriptomic Profiling of Cardiac Hypertrophy and Fatty Heart Induced by Long-Term High-Energy Diet in Bama Miniature Pigs.
Li et al., Beijing, China. In Plos One, 2014
Quantitative RT-PCR assays identified several important differentially expressed heart-related genes, including STAT3, ACSL4, ATF4, FADD, PPP3CA, CD74, SLA-8, VCL, ACTN2 and FGFR1, which may be targets of further research.
Energy Metabolism Disorder as a Contributing Factor of Rheumatoid Arthritis: A Comparative Proteomic and Metabolomic Study.
Wang et al., Wenzhou, China. In Plos One, 2014
The verification of different proteins identified in our previous proteomic study shows that the enzymes of anaerobic catabolism were up-regulated (PFKP and LDHA), and the enzymes of aerobic oxidation and fatty acid oxidation were down-regulated (CS, DLST, PGD, ACSL4, ACADVL and HADHA) in RA patients.
Peroxisomal acyl-CoA synthetases.
Ellis et al., Baltimore, United States. In Biochim Biophys Acta, 2012
Of the 26 acyl-CoA synthetases encoded by the human and mouse genomes, only a few have been reported to be peroxisomal, including ACSL4, SLC27A2, and SLC27A4.
A novel role of brain-type ACS4 isotype in neuronal differentiation.
Cho, Puch'ŏn, South Korea. In Biochem Biophys Res Commun, 2012
These results indicate that the ACS4 protein specifically expressed in brain plays an important role in arachidonate metabolism and neuronal differentiation in the brain.
Tyrosine phosphatase SHP2 regulates the expression of acyl-CoA synthetase ACSL4.
Cornejo Maciel et al., Buenos Aires, Argentina. In J Lipid Res, 2011
the involvement of SHP2 activity in the regulation of the expression of the fatty acid-metabolizing enzyme ACSL4
Fine mapping of Xq11.1-q21.33 and mutation screening of RPS6KA6, ZNF711, ACSL4, DLG3, and IL1RAPL2 for autism spectrum disorders (ASD).
Järvelä et al., Helsinki, Finland. In Autism Res, 2011
A total of six novel and 11 known single nucleotide polymorphisms were identified. Further studies are warranted to analyze the candidate genes at Xq11.1-q21.33.
Long-chain acyl-CoA synthetase 4 modulates prostaglandin E₂ release from human arterial smooth muscle cells.
Bornfeldt et al., Seattle, United States. In J Lipid Res, 2011
CSL4 modulates PGE release from human erial smooth muscle cells.
Valproate uncompetitively inhibits arachidonic acid acylation by rat acyl-CoA synthetase 4: relevance to valproate's efficacy against bipolar disorder.
Modi et al., Bethesda, United States. In Biochim Biophys Acta, 2011
VPA's ability to inhibit Acsl4 activation of AA and of DHA to their respective acyl-CoAs, when related to the higher catalytic efficiency of AA than DHA conversion, may account for VPA's selective reduction of AA turnover in rat brain phospholipids
X linked mental retardation: a clinical guide.
Raymond, Cambridge, United Kingdom. In J Med Genet, 2006
Secondly, the relative prevalence of genes causing only non-syndromic mental retardation (IL1RAPL1, TM4SF2, ZNF41, FTSJ1, DLG3, FACL4, PAK3, ARHGEF6, FMR2, and GDI) is summarised.
[Non-specific X-linked mental retardation].
Martínez-Castellano, Valencia, Spain. In Rev Neurol, 2006
Other types of functions of the known genes include establishing and modulating synapses (DLG3, IL1RAPL, NLGN4X, GDI1), regulating transcription (ZNF41, ZNF81, PQBP1) translation (FTSJ1), and fatty acid metabolism (FACL4), etc. CONCLUSIONS: Each gene that has been identified only accounts for a minor fraction of the total amount of XLMR, and even if taken together they still do not explain half the cases of non-specific XLMR.
Non-syndromic X-linked mental retardation: from a molecular to a clinical point of view.
Meloni et al., Siena, Italy. In J Cell Physiol, 2005
The function of four proteins (ACSL4, AT2, SLC6A8, and SAP102) could not be reconciled to a common pathway.
[Monogenic causes of nonspecific X-linked mental retardation molecular aspects].
Mazurczak et al., Warsaw, Poland. In Med Wieku Rozwoj, 2002
Eight genes involved in nonspecific X-linked mental retardation have been identified so far, including FMR2, GDI1, OPHN1, PAK3, ARHGEF6, IL1RAPL, TM4SF2, and FACL4.
FACL4, encoding fatty acid-CoA ligase 4, is mutated in nonspecific X-linked mental retardation.
Renieri et al., Siena, Italy. In Nat Genet, 2002
FACL4, encoding fatty acid-CoA ligase 4, is mutated in nonspecific X-linked mental retardation
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